Neuroaxonal dystrophy in a rottweiler pup

An 8-month-old Rottweiler pup was evaluated for neurologic disorder. Clinical signs included ataxia, hypermetria of all 4 limbs, intention tremors of the head, lack of a menace reflex bilaterally, and mild proprioceptive deficits. The pup was euthanatized because of the progressive nature of the disease. Histopathologic findings consisted of decreased numbers of Purkinje cells in the cerebellum and moderate numbers of axonal spheroids in the nucleus cuneatus. This latter finding confirmed the diagnosis of neuroaxonal dystrophy.     

Babesiosis in a litter of pups

Babesia canis infection was diagnosed in a litter of seven 3-week-old Mastiff pups kept in a north Florida kennel. The pups were evaluated because of poor weight gain; the smallest pup also was markedly lethargic. Six of the pups were anemic and thrombocytopenic. A positive linear correlation between PCV and absolute reticulocyte count suggested that the variation in PCV may have been related more to the ability of a pup to increase erythrocyte production than to a difference in magnitude of erythrocyte destruction. All pups recovered from clinical signs and hematologic abnormalities attributable to babesiosis within 2.5 weeks after treatment with diminazene aceturate. Transient neurologic signs observed in 1 pup 3 days after treatment were believed to represent an adverse drug reaction. The dam of the litter had a serum titer of 1:640 for B canis, but appeared healthy, as did approximately 30 other adult dog in the kennel. The strain of B canis infecting dogs in the kennel caused severe illness and death in some pups, but clinically inapparent disease in adult dogs.     

Magnetic resonance imaging findings of neuroaxonal dystrophy in a papillon puppy

A 3.5-month-old papillon puppy was brought to our clinic with chief complaints of progressive quadriparesis, ataxia and head tremor. Lesions in the cerebellum, brainstem and spinal cord were suspected on the basis of a neurological examination. No abnormality was found in a clinicopathological examination or on magnetic resonance imaging. On the basis of these results differential diagnoses including an inflammatory disease, a degenerative condition or a storage disorder were considered. Subsequently, the signs progressed and glossoplegia and dysphagia developed at six months of age. At a second magnetic resonance imaging, severe atrophy of the entire brain was found. After these examinations, the puppy was euthanased and histopathologically diagnosed with neuroaxonal dystrophy. Because magnetic resonance imaging detected abnormal features that were characteristic of neuroaxonal dystrophy in this case, we speculate that magnetic resonance imaging can assist in the pre-mortem diagnosis of this disease.     

Coronavirus infection in a litter of pups

Summary

An outbreak of a coronavirus infection in a litter of 10‐week‐old poodle pups from a commercial kennel is described. Coronavirus‐like particles were demonstrated by electron microscopy in the intestinal contents and in the colonic mucosa. Treponemas and campylobacters were excreted in great numbers in the faeces. The gastrointestinal disturbances were complicated by hepatic and renal degeneration and severe bronchopneumonia.     

Coronavirus infection in a litter of pups

Summary An outbreak of a coronavirus infection in a litter of 10-week-old poodle pups from a commercial kennel is described. Coronavirus-like particles were demonstrated by electron microscopy in the intestinal contents and in the colonic mucosa. Treponemas and campylobacters were excreted in great numbers in the faeces. The gastrointestinal disturbances were complicated by hepatic and renal degeneration and severe bronchopneumonia.     

Muscular dystrophy in pups

Abstract

Extract

Muscular dystrophies (white muscle disease) do not appear tot be commonly encountered in the dog. Elvehjem et al. (1944) Cocks, L. V. and van Rede, C. 1966. Laboratory Handbook for Oil and Fat Analysts, 109–109. New York: Academic Press.  [Google Scholar] described the occurrence of a vitamin E-responsive muscular dystrophy in pups born to, bitches fed evaporated milk fortified with iron, copper manganese and cold liver oil. In New Zealand Money et al. (1971) Elvehjem, C. A., Gonce, J. E. and Newell, G. W. 1944. The effect of vitamin E on reproduction in dogs on milk diets. J. Pediatrics, 24: 436–441.  [Google Scholar] recorded an, advanced cardiac myopathy in a 2-week-old pup from a litter of three all of which had died after exhibiting signs of respiratory distress. Response to vitamin E treatment in a subsequently similar clinical disorder suggests that the pathological condition was probably due to a vitamin E deficiency Manktelow (1963) Hartley, W. J. 1967. Symposium: Selenium in Biomedicine, Westport, Conn.: O. H. Muth, Avi. Chapter 5 [Google Scholar], however, suggested that the disorders he had seen were possibly selenium-respoasive myopathies since they occurred in an area where ovine selenium-responsive disorders also occurred. His cases included an adult working dog that had lost the use of its hindquarters and two litters of young pups in which myocardial necrosis was the main lesion. This note is to record the occurrence of muscular dystrophy in a litter of four crossbred pups born to a bitch with a previously good breeding history.     

Neuroaxonal dystrophy of the accessory cuneate nucleus in horses

Data were collected from 37 horses with a neurologic disability and compared to a group of 34 normal horses. Affected horses had neuroaxonal dystrophy, gliosis, vacuoles, and sometimes pigment localized to the accessory cuneate nuclei with minimal or no changes in the spinal cord and no changes in the proximal peripheral nerves. The focal nature of the change and usual absence of significant light microscopic spinal cord or peripheral nerve changes are different than previously described equine neuropathologic conditions.     

Neurological diseases of rottweilers: Neuroaxonal dystrophy and leukoenceph- alomalacia

Neuroaxonal dystrophy (NAD) and leukoencephalomalacia (LEM) are two neurological disorders of the rottweiler that initially present as ataxia of all four limbs. Disorders to be included in the differential diagnosis are caudal cervical spondylomyelopathy, canine distemper virus meningoencephalomyelitis, other nervous system infections or inflammations and spinal cord neoplasia. All diagnostic tests including myelography, cerebrospinal fluid analysis, electrodiagnos-tic testing and serum and cerebrospinal fluid titres for canine distemper virus are normal in NAD and LEM. There is no treatment for either disease and neurological signs progressively deteriorate. Eventually neurological deficits develop besides ataxia and these help differentiate NAD from LEM. Dogs with NAD develop head tremors and nystagmus while dogs with LEM develop conscious proprioceptive deficits and quadriparesis; the short term prognosis for NAD is better than LEM. Most dogs with LEM are euthanased because of non-ambulatory tetraparesis within one year. The histopathological lesions associated with NAD include axonal spheroids in many spinal cord and caudal brainstem nuclei and reduced numbers of Purkinje cells in the cerebellum, while in LEM, multifocal areas of demyelination and malacia of the spinal cord and brainstem are the primary histopathological lesions. Both NAD and LEM are suspected to have an autosomal recessive genetic transmission.     

Neuroaxonal dystrophy in raccoons (Procyon lotor) from Iowa.

During a 12-month period (1998-1999), microscopic evidence of neuroaxonal dystrophy (NAD) in medullae oblongata of raccoons (Procyon lotor) was observed in 17/39 (47% prevalence in adults) from Iowa, USA. Three of the animals were kits (<3 months), 26 were between 1 and 2 years, and 10 were over 7 years. Lesions were not seen in the medullae of the 3 kits. In young adults, the lesions were mild and were seen in 7 animals. More severe lesions were present in the 10 older raccoons. Grossly, the brains were unremarkable. Microscopically, NAD was confined to the dorsal caudal medulla, where certain nuclei (predominantly gracilis and cuneate) were bilaterally affected. Severely affected animals had vacuolar degeneration of neurons or neuronal loss and extensive areas of spongiosis. Tests for the presence of PrP(res) in the brain were negative. Spongiotic areas often contained axonal spheroids. Degenerate neurons and axons occasionally contained amphophilic periodic acid-Schiff-positive granular material. There was a paucity of inflammatory cells in the affected areas. Since lesions were not present in kits, were either absent or mild in young adults, and were severe in older raccoons, the findings may be related to advancing age. Neuroaxonal dystrophy has not been previously reported in raccoons. Retrospective examination of raccoon brains from the eastern and northwestern areas of the country revealed very low prevalence of NAD. Because of the apparently high prevalence of this condition at this geographic location, factors other than age (genetic, nutritional, and/or environmental) may influence this degenerative process in the brains of raccoons in Iowa.     

Syndactyly in a litter of cats

In this case report, we describe the clinical and radiographic features of a litter of kittens affected with complex syndactyly. We also provide guidelines for the diagnosis, possible treatment and prevention of propagation of this condition. This is the first report of syndactyly in a litter of kittens and syndactyly affecting both the pectoral and pelvic limbs.